EGR2
- Known as:
- EGR2
- Catalog number:
- 000412A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- EGR2
Related genes to: EGR2
- Gene:
- EGR2 NIH gene
- Name:
- early growth response 2
- Previous symbol:
- KROX20
- Synonyms:
- -
- Chromosome:
- 10q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-31
- Date modifiied:
- 2019-04-23
Related products to: EGR2
Related articles to: EGR2
- Migraine is a chronic neurological disorder. As a classic formula for promoting blood circulation and removing blood stasis, Xuefu Zhuyu Decoction (XFZYD) has shown definite clinical efficacy in the treatment of migraine with blood stasis syndrome; however, its biological mechanisms have not yet been fully elucidated and warrant further investigation. Therefore, in this study, we employed untargeted metabolomics, combined with transcriptomic sequencing, to identify endogenous differential metabolites in plasma and differentially expressed genes in brain tissue that were significantly regulated by XFZYD in migraine rats. We further explored the key targets and potential therapeutic mechanisms involved. Through integrated multi-omics analysis, the MAPK/ERK signaling pathway was ultimately identified as the key pathway regulated by XFZYD. Molecular biology experiments further confirmed that XFZYD modulated the expression of genes involved in inflammation, vascular function, and stress response within this pathway, acting on key genes such as COX-2, P-ERK1/2, Nr4a1, and Egr2, thereby intervening in two core pathological processes: vascular dysfunction and neurogenic inflammation. In summary, from both the transcriptomic and terminal metabolic levels, this study systematically elucidated the multidimensional mechanisms by which XFZYD treats migraine by reversing the "blood stasis" state and exerting its effect of "promoting blood circulation and removing blood stasis," thereby providing new research directions and a theoretical basis for its clinical application. - Source: PubMed
Publication date: 2026/04/26
Zhu Ting-TingWang Zhu-JunRen Ke-KeLiu Wen-DuanXiao Long-JinFeng Yu-LinYang Shi-LinOuyang Hui - T cells expressing the γδ T cell receptor (TCR) develop in a stepwise process initiating at the αβ/γδ T cell branch point, followed by maturation and acquisition of effector functions, including the ability to produce interleukin-17 (IL-17) as γδT17 cells. Previous studies linked TCR signal strength and fate choices to the transcriptional regulator HEB () and its antagonist, Id3, but how these factors regulate different stages of γδ T cell development has not been determined. We found that immature fetal γδTCR cells from conditional knockout (HEB cKO) mice were defective in activating the γδT17 program at an early stage, whereas -deficient (Id3-KO) mice displayed a partial block in γδT17 maturation and a defect in IL-17 production. We also found that HEB cKO mice failed to upregulate during γδT17 development, whereas HEB overexpression elevated the levels of in collaboration with TCR signaling. Moreover, Egr2 and HEB were bound to several of the same regulatory sites on the gene locus in the context of early T cell development. Therefore, our findings reveal an interlinked sequence of events during which HEB and TCR signaling synergize to upregulate , which enables maturation and acquisition of the γδT17 effector program. - Source: PubMed
Publication date: 2026/04/22
Selvaratnam Johanna Sda Rocha Juliana D BRajan VinothkumarWang HelenReddy Emily CGams Miki SLiu Jenny JiahuanMurre CornelisWiest DavidGuidos Cynthia JZúñiga-Pflücker Juan CarlosAnderson Michele Kay - Mixed stroke, also known as hemorrhagic infarction or infarction with hemorrhage, presents as a cerebral infarction combined with intracerebral hemorrhage (ICH) on computed tomography (CT) brain scans. ICH is a brain parenchymal hemorrhage caused by the loss of vascular integrity, which can lead to permanent disability or death. The early growth response 2 (EGR2) gene has been studied in a variety of brain diseases. However, effective treatments are still lacking. - Source: PubMed
Publication date: 2026/04/09
Zhang XiujunZhang BensiShi ChunKampan NatnichaTreebupachatsakul WaleephanPantan RungusaNarakornsak SuteeraPhatsara Manussabhorn - Rare earth elements (REE), such as gadolinium (Gd) and erbium (Er), are increasingly recognised as emerging environmental contaminants due to their widespread use in industrial processes, electronics, and medical imaging applications. Despite their extensive presence in aquatic ecosystems, little is known about their developmental toxicity. In this study, embryos were exposed to environmentally relevant concentrations of Gd and Er during critical early developmental stages. The assessed endpoints included survival, malformations, growth (body length), and heart rate. Both Gd and Er caused significant sublethal effects, including increased axial malformations, reduced growth, and altered cardiac activity. To explore potential mechanisms of toxicity, the expression patterns of key developmental genes (, , , , , ) and pro-inflammatory cytokines (, , ) were analysed using Real-Time PCR. The results showed dysregulation of gene expression, indicating disruption to pathways involved in morphogenesis and neurodevelopment. Elevated reactive oxygen species levels suggested that oxidative stress was a contributing factor. Raman spectroscopy confirmed biochemical changes affecting proteins, lipids, and nucleic acids, providing evidence of cellular stress and metabolic imbalance. Overall, our findings demonstrate that even low-level exposure to Gd and Er can impair amphibian embryonic development and disturb molecular homeostasis. These results emphasise the ecological risks of REE pollution and highlight the importance of ongoing environmental monitoring and long-term toxicological research. - Source: PubMed
Publication date: 2026/03/24
Fogliano ChiaraDi Marino SimonaRusciano GiuliaVignola FrancescaPetito AdrianaVenditti PaolaCretì PatriziaMotta Chiara MariaAvallone BiceScudiero RosariaCarotenuto Rosa - Tau neurofibrillary tangles are a hallmark of several neurodegenerative diseases called tauopathies, including frontotemporal dementia and Alzheimer's Disease. Ongoing clinical trials for tauopathies seek to reduce Tau in the brain through immunotherapy, antisense oligonucleotides, and siRNA. codes for Tau, therefore understanding how the gene is regulated and the effect of genetic variation at its regulatory elements is likely to have high relevance for tauopathies. We screened a ~3 Mb region including the locus using 2 different massively parallel reporter assay (MPRA) strategies in KOLF2.1J h-NGN2 neurons and HEK293FT cells, identifying previously unannotated cis-regulatory elements (CREs). Using CRISPR interference (CRISPRi) in mixed neuron cultures, we identified a new CRE for , as well as 2 CREs for another nearby gene of interest, . Known genetic variation from the Alzheimer's Disease sequencing project was tested in a separate MPRA at the top CREs near the gene, identifying variants with altered regulatory effects including those at previously identified CREs for . Using a saturation mutagenesis screen of a 2,000 bp region encompassing the promoter, we assessed regulatory effects of each possible single nucleotide variant in this region. We identified several neuron-specific regulatory variant effects at this region, including a high confidence binding site for the transcription factors EGR2, ZBTB14, and TCLF5 at a region of high MPRA activity and genetic conservation. - Source: PubMed
Publication date: 2026/03/09
Hauser Rebecca MLimbo Henry LBrazell J NicholasMoyers Belle ALauzon Shelby NBarinaga Erin AJohnston S QuinnRogers Brianne BTaylor Jared WCochran J Nicholas